text: Individual progeny genomes are excised from genomic replicative concatemers starting by introducing breaks in replication origins, usually by the replication initiator protein. This results in the establishment of new replication forks that replicate the telomeres in a combination of terminal resolution and junction resolution and displaces individual ssDNA genomes from the replicative molecule. At the end of this process, the telomeres are folded back inwards to form hairpins on excised genomes. The extended-form termini created during excision resemble the extended-form molecules prior to terminal resolution, so they can be melted out and refolded into rabbit ears for additional rounds of replication. Within an infected cell, numerous replicative concatemers are therefore able to arise.
  Displacement of progeny ssDNA genomes either occurs: predominantly or exclusively during active DNA replication, or when cells are assembling viral particles. Displacement of single strands may therefore be associated with packaging viral DNA into capsids. Earlier research suggested that the preassembled viral particle may sequester the genome in a 5′-to-3′ direction as it is displaced from the fork, but more recent research suggests that packaging is performed in a 3′-to-5′ direction driven by the NS1 helicase using newly synthesized single strands.
  It is not clear if these single strands are released into the nucleoplasm so that packaging complexes are physically separate from replication complexes or if the replication intermediates serve as both replication and packaging substrates. In the latter case, newly displaced progeny genomes would be kept in the replication complex via interactions between their 5′-linked NS1 molecules and NS1 or capsid proteins that are physically associated with replicating DNA. Genomes are inserted into the capsid via an entrance called a portal situated at one of the icosahedral 5-fold axes of the capsid, which is possibly opposite of the opening from which genomes are expelled early in the replication cycle.
  Strand selection for encapsidation likely does not involve specific packaging signals but may be predictable by the Kinetic Hairpin Transfer (KHT) mathematical model, which explains the distribution of the strands and terminal conformations of packaged genomes in terms of the efficiency with which each terminus type can undergo reactions that allow it to be copied and reformed. In other words, the KHT model postulates that the relative efficiency with which two genomic termini are resolved and replicated determines the distribution of amplified replication intermediates created during infection and ultimately the efficiency with which ssDNAs of characteristic polarity and terminal orientations are excised, which will then be packaged with equal efficiency.
  Preferential excision of particular genomes is only apparent during packaging. Therefore, among parvoviruses that package strands of one sense, replication appears to be biphasic. At early times, both sense strands are excised. This is followed by a switch in the replication mode that allows for exclusive synthesis of a single sense for packaging. A modified form of the KHT model, called the preferential strand displacement model, proposes that the aforementioned switch in replication is caused by the onset of packaging because the substrate for packaging is probably a newly displaced DNA molecule. For heterotelomeric parvoviruses, imbalance of origin firing leads to preferential displacement of negative sense strands from the right-end origin. The relative frequency of sense strands in packaged virions can therefore be used to infer the type of resolution mechanism used during excision.
  Shortly after the start of S-phase, translation of viral mRNA leads to the accumulation of capsid proteins in the nucleus. These proteins form into oligomers that are assembled into intact empty capsids. After encapsidation, complete virions may be exported from the nucleus to the exterior of the cell before disintegration of the nucleus. Disruption of the host cell environment may also occur later on in infection. This results in cell lysis via necrosis or apoptosis, which releases virions to the outside of the cell.